Moderator: Moderators
Pesticide chemical or class matrix score
Diuron 1.812
Glyphosate 1.395
Imidacloprid 0.997
Organochlorine 2.377
Akton 1.856
Guthion 2.826
Bensulide (shown above) 6.325
Dieldrin 0.8012
Diactyl 7.454
Carbamate 1.052
Atrazine 3.709
Pyrethrin 1.150
ACE inhibitors 29.313
It certainly looks like AcetylCholineEsterase inhibitors used as pesticides are used closer to to bat foraging areas than all of the others, and may need further investigation. This type of biological activity (ACE inhibition) would cause bats to burn off fat faster than normal. It might be detectable if animals were tested during foraging.
peter febb wrote:Pesticide chemical or class matrix score
Diuron 1.812
Glyphosate 1.395
Imidacloprid 0.997
Organochlorine 2.377
Akton 1.856
Guthion 2.826
Bensulide (shown above) 6.325
Dieldrin 0.8012
Diactyl 7.454
Carbamate 1.052
Atrazine 3.709
Pyrethrin 1.150
ACE inhibitors 29.313
It certainly looks like AcetylCholineEsterase inhibitors used as pesticides are used closer to to bat foraging areas than all of the others, and may need further investigation. This type of biological activity (ACE inhibition) would cause bats to burn off fat faster than normal. It might be detectable if animals were tested during foraging.
I processed the last item this morning. This is an expected finding -- something that was readily predictable from the early descriptions of the syndrome. This result clearly shows that ACE inhibitors are used in areas where bat fatalities are documented. These chemicals have short half-lives and are not likely to be found during hibernation.
peter febb wrote:Brian, I don't believe for one minute that pesticides are causing the fungus to spread, or that WNS is only found where ACE-pesticides are used. Instead, I expect pesticide concentrations and chemical classes will modify the fatality rate from WNS, and that the fungus is but one of several elements involved.
What might have a more direct effect on the fungus would be something that suppresses the immune system, even if only a little bit. Even something as subtle as lowered nutrition can be a player in this game:
"...Working with organochlorine, organophosphate and carbamate compound, we have found that: (1) dietary protein deficiency makes the immune system more susceptible to the toxic effects of pesticides; (2) suppression of immune responses by the immediate metabolites is an important determinant of the toxicity of parent compound; (3) the type and duration of physical or emotional stress and possible involvement of free radicals (oxidative stress) are important in the potentiation of pesticide-induced immune toxicity. An understanding of these risk factors depends largely upon the cellular and molecular events underlying pesticide-induced immune alterations in experimental animals. These factors, therefore, must be considered in the safety/toxicity evaluation of any pesticide. This paper reviews the influence of these factors on the immune-toxicity of some common pesticides." (The influence of various factors on immune toxicity assessment of pesticide chemicals, B. D. Banerjee, Toxicology Letters Volume 107, Issues 1-3, 30 June 1999, Pages 21-31)
Carbamates, organochlorines, organophosphates, pyrethrins, and Atrazine are all known to have immuno-suppressive effects on mammals. Atrazine is one of the herbicides that I first identified as being in the "hotzone" in 2005.
peter febb wrote:Brian, I don't believe for one minute that pesticides are causing the fungus to spread, or that WNS is only found where ACE-pesticides are used. Instead, I expect pesticide concentrations and chemical classes will modify the fatality rate from WNS, and that the fungus is but one of several elements involved.
What might have a more direct effect on the fungus would be something that suppresses the immune system, even if only a little bit. Even something as subtle as lowered nutrition can be a player in this game:
"...Working with organochlorine, organophosphate and carbamate compound, we have found that: (1) dietary protein deficiency makes the immune system more susceptible to the toxic effects of pesticides; (2) suppression of immune responses by the immediate metabolites is an important determinant of the toxicity of parent compound; (3) the type and duration of physical or emotional stress and possible involvement of free radicals (oxidative stress) are important in the potentiation of pesticide-induced immune toxicity. An understanding of these risk factors depends largely upon the cellular and molecular events underlying pesticide-induced immune alterations in experimental animals. These factors, therefore, must be considered in the safety/toxicity evaluation of any pesticide. This paper reviews the influence of these factors on the immune-toxicity of some common pesticides." (The influence of various factors on immune toxicity assessment of pesticide chemicals, B. D. Banerjee, Toxicology Letters Volume 107, Issues 1-3, 30 June 1999, Pages 21-31)
Carbamates, organochlorines, organophosphates, pyrethrins, and Atrazine are all known to have immuno-suppressive effects on mammals. Atrazine is one of the herbicides that I first identified as being in the "hotzone" in 2005.
Bayer Crop Science started petitioning the agency to approve a new pesticide for sale in 2006. After reviewing the company's studies of its effects on bees, the EPA gave Bayer conditional approval to sell the product two years later, but said it had to carry a label warning that it was "potentially toxic to honey bee larvae through residues in pollen and nectar.
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